摘要
Objective: To elucidate the pattern of chemo therapy drugs induced apoptosis and its role in chemo therapy of acute leukemia. Methods: Apoptosis induced by Ara C in human myeloid leukemia cell line HL 60 was investigated by applying light microscope, electron microscopy combined with DNA electrophoresis and flow cytometry analysis techniques. Results: Apoptosis per sisted throughout 36 h following addition of Ara C with a gradual augmentation. Efficiency of apoptosis was enhanced in a dosedependent pattern, HL 60 treated with six other chemotherapy drugs and peripheral white blood cells from a AML case undergoing DA regimen chemo therapy exhibited typical DNA ladder pattern. Further investigation indicated that chemotherapy drugs apop tosis came into being possibly by downregulating the expression of c myc and bcl 2 oncogenes. Conclusion: Chemotherapy induced apoptosis is the primary mecha nism of chemotherapy.
Objective: To elucidate the pattern of chemo therapy drugs induced apoptosis and its role in chemo therapy of acute leukemia. Methods: Apoptosis induced by Ara C in human myeloid leukemia cell line HL 60 was investigated by applying light microscope, electron microscopy combined with DNA electrophoresis and flow cytometry analysis techniques. Results: Apoptosis per sisted throughout 36 h following addition of Ara C with a gradual augmentation. Efficiency of apoptosis was enhanced in a dosedependent pattern, HL 60 treated with six other chemotherapy drugs and peripheral white blood cells from a AML case undergoing DA regimen chemo therapy exhibited typical DNA ladder pattern. Further investigation indicated that chemotherapy drugs apop tosis came into being possibly by downregulating the expression of c myc and bcl 2 oncogenes. Conclusion: Chemotherapy induced apoptosis is the primary mecha nism of chemotherapy.
